Laboratory of Cellular and Molecular Neurobiology, School of Life Sciences, Jawaharlal Nehru University, New Delhi, 110067, Delhi, India.
Mol Neurobiol. 2022 Jul;59(7):4466-4487. doi: 10.1007/s12035-022-02867-7. Epub 2022 May 16.
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by hyperglycemic conditions. A higher risk of developing Parkinson's disease (PD) in patients with T2DM has become evident in recent years. However, the molecular mechanisms underlying the interplay between T2DM and PD pathogenesis remain unknown. Nevertheless, emerging epidemiological studies have demonstrated many common molecular pathways that play an essential role in regulating normal cellular functioning are independently implicated in the progression and etiopathogenesis of T2DM and PD. This review summarizes some common shared pathophysiological mechanisms, including insulin resistance, inflammation, mitochondrial dysfunction, endoplasmic reticulum stress (ER stress), autophagy, and the ubiquitin-proteasome system (UPS) that independently mediate the onset and etiopathogenesis of T2DM and PD. In this review, we summarize the studies that have reported the relationship between T2DM and PD. This review will provide insights into the common involvement of molecular pathways that may provide alternative treatment strategies for both T2DM and PD.
2 型糖尿病（T2DM）是一种以高血糖为特征的慢性代谢性疾病。近年来，T2DM 患者患帕金森病（PD）的风险明显增加。然而，T2DM 和 PD 发病机制之间相互作用的分子机制尚不清楚。然而，新兴的流行病学研究表明，许多在调节正常细胞功能中起重要作用的共同分子途径，独立地参与了 T2DM 和 PD 的进展和发病机制。这篇综述总结了一些常见的共同病理生理机制，包括胰岛素抵抗、炎症、线粒体功能障碍、内质网应激（ER 应激）、自噬和泛素-蛋白酶体系统（UPS），这些机制独立介导 T2DM 和 PD 的发病和发病机制。在这篇综述中，我们总结了报道 T2DM 和 PD 之间关系的研究。这篇综述将为分子途径的共同参与提供深入了解，这可能为 T2DM 和 PD 提供替代治疗策略。
